Several studies using SHRs failed to demonstrate the pressor effect of alcohol. In other studies chronic alcohol administration resulted in the attenuation of the development of hypertension in SHR or stroke-prone SHR. Although it was shown that alcohol administration caused a mild reduction in blood pressure still the mechanism of action is not understood. Indirect evidence from human studies had shown that the pressor effect of acute and chronic alcohol consumption may be due to the alteration of intracellular calcium accumulation. Preliminary studies suggest that chronic alcohol consumption in WKY and SH rats suppresses blood pressure, heart rate, and increased histamine levels which may involve a shift in intracellular calcium or increased entry of calcium into cardiovascular vessels through the regulation of voltage- activated calcium channels. However, the involvement of chronic alcohol consumption on the alteration of intracellular Ca2+ in hypertensive individuals is not clearly understood. We hypothesize that the tolerance and desensitivity of cardiovascular vessels to chronic alcohol exposure is mediated by changes in calcium transport into vascular smooth muscle. To test this hypothesis the following studies were proposed: 1. Effects of chronic and acute ethanol exposure on Ca2+ transients in SHR and WKY arterial (aorta rings) smooth muscle will be investigated. (Hypothesis: Chronic ethanol exposure affects the intracellular accumulation of Ca2+ in vascular smooth muscle of SH rats). 2. Data from Ca2+ influx of arterial smooth muscle will be correlated with data from the effects of ethanol on heart rate, mean arterial blood pressure, and histamine levels of chronic and acute exposed SHR and WKY rats. (Hypothesis: Chronic ethanol exposure alters the Ca2+ transport mechanism in vascular smooth muscle affecting blood pressure, heart rate, and histamine levels. 3. Changes in responsiveness of vascular smooth muscle (aorta) of SHR and WKY rats to chronic and acute ethanol exposure will be studied. (Hypothesis: Chronic alcohol (ethanol) exposure augments Ca2+ efflux affecting the relaxation of vascular smooth muscle in SH rats).